Volkan-Salanci Bilge, Dagdelen Selcuk, Alikasifoglu Mehmet, Erbas Tomris, Hayran Mutlu, Erbas Belkis
Department of Nuclear Medicine, Faculty of Medicine, Hacettepe University, Ankara, Turkey.
J Renin Angiotensin Aldosterone Syst. 2009 Mar;10(1):41-50. doi: 10.1177/1470320309102326.
The aim of this study was to document the impact of renin-angiotensin system (RAS) polymorphisms on renal haemodynamics and renal hormones in type 2 diabetes mellitus.
Fifty-nine adult patients were studied. Renal haemodynamics were evaluated using 99mTc-MAG3 clearance (MAG3( Cle)) using Bubeck's method and captopril renogram. RAS hormones and angiotensin-converting enzyme (ACE) levels were measured before and after captopril.ACE, angiotensin II type 1 receptor and angiotensinogen gene polymorphisms were analysed.
Post-captopril MAG3(Cle) values were significantly lower in patients with microalbuminuria compared to nonproteinuric patients. Statistically significant negative correlation was found between clearance percentage change values and HbA(1c) levels (r: -0.42, p=0.009). MAG3(Cle) was relatively lower following captopril administration in DD patients, while a relative increment was observed in I allele carriers (p=0.02).TheAC-CC group had significantly higher mean post-captopril clearance value compared to the AA genotype (480.9+/-56.1 ml/min/1.73 m(2) vs. 428.4+/-74.8 ml/min/1.73 m(2), p=0.022).
Our data indicate that the heterogeneity of patients' response to ACE inhibition is, at least partly, genetically determined, and the genetic polymorphisms in RAS might predict the acute responsiveness to ACE inhibitors.
本研究旨在记录肾素 - 血管紧张素系统（RAS）基因多态性对2型糖尿病患者肾血流动力学和肾激素的影响。
对59例成年患者进行了研究。采用Bubeck法和卡托普利肾图，通过99mTc - MAG3清除率（MAG3（Cle））评估肾血流动力学。在服用卡托普利前后测量RAS激素和血管紧张素转换酶（ACE）水平。分析ACE、血管紧张素II 1型受体和血管紧张素原基因多态性。
与无蛋白尿患者相比，微量白蛋白尿患者服用卡托普利后的MAG3（Cle）值显著降低。清除率变化百分比值与糖化血红蛋白（HbA1c）水平之间存在统计学上显著的负相关（r：-0.42，p = 0.009）。DD基因型患者服用卡托普利后MAG3（Cle）相对较低，而I等位基因携带者则观察到相对增加（p = 0.02）。与AA基因型相比，AC - CC组服用卡托普利后的平均清除率值显著更高（480.9±56.1 ml/min/1.73 m² 对 428.4±74.8 ml/min/1.73 m²，p = 0.022）。
我们的数据表明，患者对ACE抑制反应的异质性至少部分是由基因决定的，RAS中的基因多态性可能预测对ACE抑制剂的急性反应性。
